 | Term | Definition |
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Mesosome |
coiled cytoplasmic membrane that acts as an anchor to pull apaprt daughter chromosomes during cell division |
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Why are bacterial ribosomes major targets of antibiotics |
because bacterial ribosomes 70S: 50s/30s are significantly different from eukaryotic ribosomes |
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Are steroids (cholesterol) found in bacterial membranes? |
No |
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What are the two main structural components of the peptideglycan layer |
N acetyl glucosamine and N acetylmuramic acid |
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What are the “penicillin binding proteins”? |
transpeptidases, carboxypeptidases, and endopeptidases that are involved in cell wall biosynthesis. They extend petidoglycan, create a septum for cell division and curving the peptidoglycan mesh |
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What are techoic acids? |
water soluble polymers of ribose or glycerol which may be attached to peptidoglycan (as in lipotechoic acids which are covalently attached to the cytoplasmic membrane bound fatty acid) |
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Where is LPS found? |
Gram Negative (G~) |
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What effect does LPS Produce |
activates B cells; causes release of proinflammatory cytokines, fever, and shock |
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What are the three components of LPS |
Lipid A, Core, O~antigen |
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What are the 2 most abundant components of the outer membrane? |
Phospholipids (highest), LPS (next highest) |
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Do Gram neg or Gram pos undergo sporulation? |
Gram + |
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What are the three functions of capsules? |
the carb or protein surface layer, 1) physical barrier 2) inhibition of phagocytosis by complement deposition interruption 3) mediate immune invasion by mimicking host glycans |
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What is a useful property of the flagella? |
it can be a serodeterminant in the H serotyping scheme |
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Regarding flagella, counterclockwise (CCW) rotation does what? |
CCW propels the organism forward, unlike CW rotation which allows the bacteria to “tumble” and reorient its direction |
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What is the basis of serological typing schemes and what are the three main types? |
surface antigens form the basis and the types are “O” ~somatic (LPS) “H” ~flagellar “K” ~capsular |
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What is a biofilm? |
a protective mode of growth consisting of a self-produced polymeric matrix which allows survival in hostile environments by providing resistance to host defenses and antibiotics |
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What are the human infections involving biofilms? |
periodontitis, cystic fibrosis, chronic bacterial prostatitis, otitis media, Native valve endocarditis |
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What occurs first when bacteria interact with Cells |
the LPS, glucan, or manose receptors identify the bacteria or toxin and release cytokines |
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What cytokines are released by receptors upon interaction with bacteria or toxins |
IL~1, IL~6, TNF alpha |
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What are examples of pyogenic bacteria and what do they cause |
Staphlococci, streptococci, neisseria; they produce purulent exudates (pus) |
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Biopsies of infected sites typical show what types of cells? |
PMN’s, Macrophages, Plasma cells, lymphocytes |
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What 2 types of patients have an increased risk for bacterial infection? |
Granulocytopenic patients, and those with chronic granulomatous disease |
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Opsonization by C3b is CRITICAL for clearance of which organisms |
Gram Positive (also effective for gram negative) |
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Bacteriolysis by the membrane attack complex (MAC) in the classical pathway is CRITICAL for clearance of which organism? |
Gram Negative (NOT effective for G+) |
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How do bacteria evade host complement? |
Capsule production (inhibit deposition of C3b), antiphagocytic proteins (binding negative regulators of the complement cascade), LPS (inhibits the insertion of MAC) |
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Give examples of antiphagocytic proteins |
M protein of S. pyogenes, porin proteins of N. gonorrhoeae, GNA1870 lipoprotein of N meningitides, Osp proteins of B burgdoreferi |
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What diseases do encapsulated bacteria more often cause |
meningitis, pneumonia, systemic infections by disseminating through bloodstream or lymphatics |
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What occurs during Gram Negative sepsis |
infection by LPS, systemic release of TNF alpha from macrophages in liver and spleen affecting all venules simultaneously, systemic edema, decreased blood volume causes collapse of vessels |
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Name the bacterial species that can grow in refrigerated food |
Listeria monocytogenes (#1 reason for food recalls) and Yersinia |
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What are fomites |
vehicles for transfer of disease and infection (towels, eating utensils…) |
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Which ones are the spore formers |
mostly G+ |
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What are obligate aerobes (name examples too) |
require O2 for growth; Mycobacterium tuberculosis, pseudomonas aeruginosa |
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Obligate anaerobes (examples?) |
O2 will kill them; clostridium tetani, clostridium botulinum |
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Microaerophilic |
grow with a small amount of O2; use aerobic respiration ;campylobacter jejuni |
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Aerotolerant |
Tolerate O2, but they use fermentation for energy; bacteroides fragilis |
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Capnophilic |
CO2 loving; strep pneumo, mycobac tuberculosis, neisseria gonorrheae |
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Facultative anaerobes |
use aerobic respiration AND fermentation; grow fastest in O2 ; E. Coli |
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What molecules terminate toxic oxygen species |
superoxide dismutase, catalase, peroxidase |
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Siderophores |
iron scavenging compound secreted by organisms |
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Pasteurization |
heat treatment b/w 62 and 74 degrees celcius to kill vegetative bacteria w/o altering food |
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What is important to remember with bacterial killing |
killing is a product of time exposure, # of organisms, and efficacy of chemical (or agent) |
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NADH provides how many ATP? |
3 |
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What method provides the most accurate measurement of bacterial growth |
Viability counts (serial 10 fold dilutions) |
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Transversion |
a base mutation where a purine is changed to a pyrimidine or vice versa |
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Degenerate |
a mutation that still codes for the same amino acid |
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Nonsense |
a mutation that encodes a stop codon |
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What are the stop codons (RNA version) |
UAA, UAG, UGA (you’re a goat…) |
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Auxotrophy |
the inability of an organism to synthesize a particular organic compound required for its growth |
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What do intercalating agents do? |
Induce frameshifts via single base pair insertions / deletions |
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Reversion |
restores the DNA sequence to the wild type |
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Suppression |
a second mutation restores the phenotype of the wild type even though the original mutation remains |
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Name the DNA repair mechanisms |
deaminated bases repaired by glycosylases; photoreactivation enzyme and UV light; Excision repair (UvrAD); methylated/ unmethylated DNA mismatch repair |
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What is the repair defect in Xeroderma pigmentosa |
fibroblasts are deficient in excision of thymidine dimmers |
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Hereditary nonpolyposis colon cancer |
loss of mismatch repair due to mutations in hMSH2 |
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Replicon |
DNA that can replicate on its own after transfer to a new host |
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Recombination |
breakage and rejoining of 2 DNA molecules to form a hybrid recombinant DNA molecule |
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Transformation |
when “naked” DNA is taken up by bacteria and incorporated into the host DNA |
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Competence |
ability to take up DNA (both G+ and G~ show competence) |
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DNA degrading enzyme |
degrades on strand of the naked DNA as it is transformed into a host |
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Specificity of transformation |
some bacteria will not take certain DNA others require a signature sequence |
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Transduction |
Gene transfer that is mediated by a bacteriophage |
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Virions |
a mature, synthesized and assembled, bacteriophage |
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Obligate parasite |
cannot live without the host |
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How do bacteria become resistant to phages? |
absence of phage receptor (phage can’t bind) |
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Abortive transduction |
when the viral DNA is not incorporated into the host and is transmitted only to one of the daughter cells |
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OriT |
transfer origin in the DNA |
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F+ |
a plasmid with only F DNA |
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F’ |
a plasmid with both F DNA and Bacterial chromosomal DNA |
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Transposition |
uses transposases to transfer a gene from donor to recipient DNA |
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LexA |
transcriptional repressor |
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What is the 3-fold basis of Abx selective toxicity? |
1) absence of the target from the host 2) permeability differences b/w host and bacteria 3) structural differences in the target |
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Intrinsic resistance |
target on which the ABx works is missing |
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Linezolid |
(zyvox) the only clinically significant drug that inhibits the 70s initiation complex; Bacteriostatic for staphylococci and enterococci, but is bacteriocidal for streptococci. |
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Bacteriostatic drugs |
competitive inhibitors with some dissociation (reversible binding to target) |
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Bacteriocidal drugs |
competitive inhibitors which irreversibly bind to target |
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Aminoglycosides |
class of Abx; each of which targets a different protein in the 30s ribosomal subunit |
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Aminoglycosides (names) |
streptomycin, kanamycin, tobramycin, gentamycin, neomycin, amikacin, paramomycin, etc…(broad spectrum, G+/-) |
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Streptomycin |
causes misreading through an A site codon distortion, causes a cyclic polysomal blockade (creates an unstable 70s subunit that falls apart, preventing translation, causes membrane changes which alter the membrane of the bacteria (leaky membranes kill the bacteria) |
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Spectinomycin |
(aminocyclitol abx) similar to streptinomyocin but only causes the formation of the unstable 70s subunit; used to treat gonorrhea when penicillin is inappropriate |
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Tetracyclins |
bacteriostatic, targets 70s, INTRACELLULAR, inhibit binding of the charged tRNA at the A site; used of the treatment of Chlamydia, mycoplasma, Rickettsia, and some G+/- organisms |
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Resistance to Tetracyclins |
1) decreased uptake often due to mutations in the OmpF porin 2) Efflux from the bacterial cell 3) Elongation factor~like proteins that protect the 30s ribosomal subunit |
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Chloramphenicol |
bacteriostatic agent which prevents peptidyl transfer of a growing bacterial peptide by binding (reversibly) to the 50s subunit |
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Chloramphenicol Resistance |
plasmid encoded acetyltransferase that catalyzes the acetylation of the OH groups which prevents 50S binding |
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Lincomycin & Clindamycin |
narrow spectrum; bacteriostatic; similar mechanism to chloramphenicol; effective for G+ infections!! (clindamycin effectively treats staphylococcal and anaerobic G- [bacteroides] infections) |
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Lincomycin & Clindamycin Resistance |
methylation of the 23S ribosomal RNA which prevents binding to the 50S ribosomal subunit |
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Macrolides |
-[azithromycin, clarithromycin, erythromycin..] bacteriostatic; effectively treat mycoplasma, legionella, chlamydia, and campylobacter; some intracellular some extracellular; and (G+ bacteria in patients allergic to penicillin) [may prevent elongation, release, or transpeptidation of bacterial proteins |
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Macrolide resistance |
1) methylation of the 23S RNA preventing 50S binding 2) hydrolysis of the lactone ring by an esterase 3) efflux of the drug |
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Ketolides |
[telithromycin] blocks exit of nascent polypeptide from the ribosome |
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Streptogramins |
[produced by a certain subclass of streptomyces] quinupristin, synercid |
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Dalfopristin |
binds to 50S ribosomal subunit and facilitates binding of quinupristin |
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Quinupristin |
premature release of peptide chains from the ribosome |
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What is synercid |
quinupristin and dalfopristin combined; together they have bactericidal properties |
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If you see a red bacteria it must be |
serratia |
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Which organisms are the Most common causes of Gram negative sepsis |
(PEEKS) Proteus, E. coli, Enterobacter, Klesiella, serratia “the patient PEEKS at death with sepsis” |
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What does the urease produced by Proteus M. cause |
kidney stones |
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What are the products of urease? And what does this cause |
CO2 and NH3 (increase pH --> stone formation) |
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What are the clinical manifestations of pyelonephritis? |
flank pain, fever, nausea vomiting, increased CRP, 30% bacteremia |
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What are the clinical manifestations of cystitis? |
dysuria, frequent urination, suprapubic pain |
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What is an uncomplicated UTI; who is most susceptible? |
clean catch midstream, >10^5 bacteria/mL single species….Women |
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What is a complicated UTI |
10^2 to10^4 Bacteria/mL, multiple species, biofilms….hospitalized patients with catheters |
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What advantage do lateral flagella give P . mirabilis in establishing pyelonephritis? |
swim better |
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How is EHEC 0157:h7 identified in the lab? |
rapid test |
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How is etec identified in the lab? |
DNA probe |
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Why are US travelers susceptible to ETEC but not EPEC? |
EPEC is age specific whereas ETEC is for those who are not immune (travelers) |
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What are the two virulence factors in UPEC? |
type 1 fimbriae (exfoliation of bladder cells) and P Pili (adhere to digalactoside receptors (p blood group) req’d for colonization of upper urinary tract |
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Mechanism of heat labile toxin (LT) |
AB Toxin; B binds to the GM1 gangliosides (same as cholera toxin); after endocytosis, A crosses the vacuole membrane and uses ADP-ribosyltransferase activity to interact with the G protein and andenylate cyclase which increases cAMP; this secretes electrolytes causes water to follow |
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Mechanism of heat stable toxin (ST) |
a small monomeric peptide which binds to the transmembrane guanylate cyclase receptor leading to increased cGMP and a hypersecretion of fluids |
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Mechanism of shiga toxin |
AB toxin; B binds to cell glycolipid and A enters the cell and cleaves the 28s rRNA subunit of the 60s ribosomal subunit, this prevent the binding of the aminoacyl tRNA thereby disrupting protein synthesis |
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What are some sources of Campylobacter infections in humans? |
contaminated food, milk, water (food that reduces the acidity of the stomach helps infection occur; lower dose needed) |
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What is needed to culture C. jejuni? |
special media w/ abx and reduced O2 and increased CO2. they appear as colorless/grey colonies (gull shaped wings) |
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